Department of Radiotheragy, The Second Affiliated Hospital of Guangxi University of Science and Technology, Liuzhou, Guangxi 545005, P.R. China.
Department of Cardiology, Huadu District People's Hospital, Southern Medical University, Guangzhou, Guangdong 510800, P.R. China.
Biosci Rep. 2020 Feb 28;40(2). doi: 10.1042/BSR20193794.
MCM3AP antisense RNA 1 (MCM3AP-AS1) is characterized as an oncogenic lncRNA in hepatocellular carcinoma and glioblastoma. We analyzed TCGA dataset and observed the down-regulation of MCM3AP-AS1 in cervical squamous cell carcinoma (CSCC). The present study was therefore performed to investigate the role of MCM3AP-AS1 in CSCC.
A total of 64 female patients with CSCC (38-68 years old; mean age: 53.1 ± 6.5 years old) were enrolled in the present study. RT-qPCR was performed to evaluate gene expression. Methylation specific PCR (MSP) was performed to assess the methylation of miR-93 gene after the overexpression and silencing of MCM3AP-AS1. Cell transfections were performed to investigate the interactions between MCM3AP-AS1 and miR-93. Cell proliferation was assessed by CCK-8 assay.
The results showed that MCM3AP-AS1 was down-regulated in CSCC and predicted poor survival. The expression levels of MCM3AP-AS1 were inversely correlated with the expression levels of miR-93. Overexpression of MCM3AP-AS1 led to down-regulation of miR-93, while silencing of MCM3AP-AS1 played an opposite role in CSCC cells. Methylation-specific PCR revealed that MCM3AP-AS1 could positively regulate the methylation of miR-93 gene. Cell proliferation analysis showed that overexpression of MCM3AP-AS1 led to reduced proliferation rate of CSCC cells. Silencing of MCM3AP-AS1 played an opposite role and overexpression of miR-93 reduced the effects of overexpressing MCM3AP-AS1.
Therefore, MCM3AP-AS1 may inhibit cell proliferation in CSCC by down-regulating miRNA-93.
MCM3AP 反义 RNA1(MCM3AP-AS1)在肝细胞癌和神经胶质瘤中被鉴定为致癌 lncRNA。我们分析了 TCGA 数据集,观察到宫颈鳞状细胞癌(CSCC)中 MCM3AP-AS1 的下调。因此,本研究旨在探讨 MCM3AP-AS1 在 CSCC 中的作用。
本研究共纳入 64 例女性 CSCC 患者(38-68 岁;平均年龄:53.1±6.5 岁)。采用 RT-qPCR 检测基因表达。采用甲基化特异性 PCR(MSP)检测 MCM3AP-AS1 过表达和沉默后 miR-93 基因的甲基化。进行细胞转染以研究 MCM3AP-AS1 和 miR-93 之间的相互作用。采用 CCK-8 法评估细胞增殖。
结果显示,MCM3AP-AS1 在 CSCC 中下调,且预测预后不良。MCM3AP-AS1 的表达水平与 miR-93 的表达水平呈负相关。MCM3AP-AS1 的过表达导致 miR-93 下调,而 MCM3AP-AS1 的沉默在 CSCC 细胞中则起到相反的作用。甲基化特异性 PCR 显示,MCM3AP-AS1 可正向调节 miR-93 基因的甲基化。细胞增殖分析显示,MCM3AP-AS1 的过表达导致 CSCC 细胞增殖率降低。MCM3AP-AS1 的沉默则起到相反的作用,过表达 miR-93 降低了过表达 MCM3AP-AS1 的作用。
因此,MCM3AP-AS1 可能通过下调 miR-93 抑制 CSCC 细胞的增殖。